Intra-muscular needle injection of therapeutic compounds is well known in the medical arts, as is intra-coronary injection where pre-existing intra-coronary arteries provide perfusate conduits. In heart disease, the existing coronary artery in-flows to capillary beds is often compromised. Newly developed gene and protein therapeutic agents hold promise in their ability to act on the surviving smaller capillary beds to grow and expand them. As has been witnessed, the intra-myocardial cellular lattice limits angiogenic response to about 5–10 mm and similar limits occur with direct needle injections in stunned or ischemid heart tissue. The physician must work within an environment of compromised capillary bed vascularity. Physicians are further limited to some degree by drug viscosity—where the drug viscosity is too-low, rapid wash-out can occur; and where too high, capillary occlusion can occur—as well as by high infusate pressure induced cellular damages. These problems are not typical of common healthy muscle tissue injections in the arm or leg. The prior art teaches the creation of permanent channels with the use of lasers, radio frequency heating and mechanical cutting means. Such channels often compromise the capillaries that are sought to be accessed with a drug, wash out readily, and resolve ultimately as fibrous connective scar tissue. Needle and membrane tools may improve access to capillaries but offer no stretching forces and don't offer unobstructed capillary access.